What specifically determines a persons abo blood group

ABH Secretors and Nonsecretors

By 1930 it had been shown that some people do and others do not secrete antigens corresponding to their ABO blood group into their saliva. Persons with these substances in saliva (secretors) have more ABH substances in their tissues than those lacking the substance in their saliva (nonsecretors). The ability to secrete behaved as a simple Mendelian function dominant to nonsecretion. Persons with blood groups A, B, and AB who are secretors secrete the antigens corresponding to their blood groups. Group H persons secrete the H substance, as do all other secretors, to a somewhat lesser extent.

ABH substances are secreted by mucous glands in many organs, including the upper respiratory tract, the gastrointestinal tract from the esophagus through the colon, and the uterine cervix. ABH secretor status is a major conditioner of the gut mucosa. ABH secretors have greater quantities of free ABH antigens in the makeup of their intestinal secretions, which has significant effects on bacterial and lectin adherence to the gut microvilli. The secretor gene regulates the synthesis of blood group substances in superficial glands of the gastric and small intestine mucosa. Large amounts of ABH material are found in all secretors,5–8 characterized by a uniform distribution of blood type antigens in the gastric pits. ABH expression is independent of secretor status: glands situated deep in the mucosa of the pylorus and small intestine (Brunner glands) and gastric parietal glands both produce A and B substances without regard to secretor status.9

For a more detailed discussion of the metabolic consequences of ABH secretor status, the reader should refer to the author’s article specifically on the subject.10

ABO Group Typing

ABO blood group phenotypes include A, B, AB, and O. Reciprocal antibodies are consistently present in the majority of individuals’ sera without previous RBC exposure (e.g., anti-B antibodies in blood group A patients), and these antibodies may result in severe intravascular hemolysis after transfusion of ABO-incompatible blood components. Prevention of ABO-incompatible transfusion is the primary objective of pretransfusion testing.

ABO is determined by testing donor RBCs with anti-A and anti-B (known as “forward” or “front” type) and donor plasma with group A1 and group B RBCs (known as “reverse” or “back” type). Discrepancies between front and back type must be resolved before labeling a blood component (Chapter 25). RBC genotyping can be used to resolve typing discrepancies.

ABO Blood Groups

ABO blood group antigens are expressed mainly on the surface of red blood cells. According to studies, non-O blood type is associated with the occurrence of MI. The underlying mechanism is related not to atherosclerotic complications but to impaired hemostasis. In particular, blood groups A and B exhibit increased levels of von Willebrand factor (VWF) compared to O blood type (VWF levels gradually decline from the AB to B to A to O blood groups) [44]. Although the detailed mechanism linking blood type to VWF is not fully elucidated, a higher half-life of VWF is found in A and B blood groups, probably due to impaired proteolysis and clearance. The risk of MI in non-O blood types is approximately 20%. Supporting the association of non-O blood groups with increased thombogenicity, A and B blood types display a twofold risk of venous thrombosis [45].

Blood Groups

ABO blood group associations were investigated in a large number of infectious diseases in early studies. An association of blood group O with increased severity of cholera symptoms was found in several studies.132,133 Blood group O is associated with peptic ulceration, which in turn is connected with H. pylori infection. A possible mechanism for this relationship was suggested by the observation that fucosylation of the Lewis b (Leb) receptor for H. pylori in the gastric mucosa, found in individuals with A or B blood group, impairs binding of the bacteria.134 However, H. pylori infection is not clearly influenced by ABO blood group type.135 Recently, a large study of Africans provided compelling evidence that blood group O associates with reduced risk of severe malaria.39

The ability to secrete blood group substances (such as secretor histo-blood group antigens, HBGA) into saliva and at other mucosal surfaces is genetically determined. Most individuals are secretors, but about 20% of most populations are nonsecretors because of mutation in the fucosyltransferase 2 (FUT2) gene.136 In relatively small studies, nonsecretion was suggested to be associated with susceptibility to some bacterial and fungal infections and with resistance to certain common viral infections.137,138 Nonsecretor status is clearly associated with susceptibility to recurrent urinary tract infection,139 and a possible mechanism for this has been proposed.140 Nonsecretor status was found to protect completely against infection with Norwalk virus in volunteer challenge studies141 and is associated with substantially reduced risk in the general population.142 More recent studies have reported symptomatic norovirus infection in nonsecretors, and in vitro binding studies have demonstrated that binding of noroviruses to HBGA is strain specific, with some norovirus strains evolving different HBGA-binding targets in an attempt to evade genetically determined host resistance.143 However, overall, apart from associations with norovirus and urinary tract infections, there is a need for larger studies to show compelling evidence of association.

The most striking blood group association is of the Duffy blood group with susceptibility to P. vivax malaria. This parasite uses the Duffy blood group antigen as the receptor to invade erythrocytes.144 The Duffy blood group antigen is a promiscuous chemokine receptor. Most sub-Saharan Africans are Duffy blood group negative because of homozygosity for a mutation in the promoter of this gene. They are completely resistant to P. vivax infection. Such individuals also express the Duffy antigen on some other tissues because the promoter mutation that is in the recognition site for an erythroid-specific enhancer is tissue specific.145 It is unclear whether the Duffy genotypes prevented P. vivax from ever entering Africa or whether an earlier and more virulent form of this parasitic infection might have selected the variant in Africa.

ABO Group Typing

The ABO blood group phenotypes include A, B, AB, and O. The reciprocal antibodies are consistently present in the sera of the majority of individuals without previous RBC exposure (e.g. anti-B antibodies in blood group A patients) and these antibodies may result in severe intravascular hemolysis after transfusion of ABO incompatible blood components. The prevention of ABO incompatible transfusion is the primary objective of pretransfusion testing.

ABO is determined by testing donor RBCs with anti-A and anti-B (also known as a ‘forward’ or ‘front’ type) and the donor plasma with group A1 and group B RBCs (also known as a ‘reverse’ or ‘back’ type). Discrepancies between the front and back type must be resolved prior to labeling a blood component (see Chapter 23). RBC genotyping can be used to resolve typing discrepancies.

ABO Group Typing:

The ABO blood group phenotypes include A, B, AB and O. The reciprocal antibodies are consistently present in the sera of a majority of individuals without previous red blood cell (RBC) exposure (e.g. anti-B antibodies in blood group A patients), and these antibodies may result in severe intravascular hemolysis after transfusion of ABO-incompatible blood components. The prevention of ABO-incompatible transfusion is the primary objective of pretransfusion testing.

ABO type is determined by testing donor RBCs with anti-A and anti-B (also known as a “forward” or “front” type) and the donor plasma with group A1 and group B RBCs (also known as a “reverse” or “back” type). Discrepancies between the front and back type must be resolved prior to labeling a blood component (see Chapters 19 and 22Chapter 19Chapter 22). RBC genotyping can be used to resolve typing discrepancies.

Transplantation in humorally sensitized recipients

Crossing ABO blood group barriers predictably results in primarily AMR, which in turn results in an increased incidence of biliary tract complications and diminished graft survival compared to ABO-compatible controls. Most North American programs, therefore, generally avoid using ABO-incompatible liver allografts, but they are still utilized in Asian programs where the donor pool is more limited. However, plasmapheresis, vigorous immunosuppression, and microcirculatory protective therapy have been used to achieve reasonable results.

Liver allografts are much less susceptible than other solid organ allografts to damage from AMR because of anti-HLA class I and II antibodies, but are not completely spared from AMR-related injury. DSA status, therefore, does not routinely influence organ triage/recipient selection at most centers, but has been associated with increased AMR and ACR rates and decreased graft survival. Living donor or reduced-size liver allografts appear to be more susceptible to AMR than whole liver cadaveric donors. This is probably related to several factors such as reduced surface for antibody absorption, smaller caliber blood vessels, and enhanced arterial vasospasm related to a combination of portal hyperperfusion and pathophysiological mediators of AMR.

ABO History

The ABO blood group was discovered by Dr. Karl Landsteiner in 1901. He was awarded the 1930 Nobel Prize for Physiology and Medicine for his landmark work in the discovery of what is still one of the most important antigen systems. In experimentation with blood from himself and his staff, he noted different patterns of agglutination between plasma and red cells. He identified these as types, which he designated as “A,” “B,” and “C” (later to be known as “O”). In 1902, his colleagues discovered the fourth main type as “AB.” His observations led to what has become known as the “Landsteiner law”: for whichever ABO antigens that are lacking on the red blood cell (RBC) surface, the corresponding antibody will be present in the serum. Therefore type A individuals have anti-B in their serum, type B individuals have anti-A, and type O individuals have anti-A and anti-B (Table 3.1). The rare Bombay phenotype individuals who lack the H-antigen have anti-A, anti-B, and anti-H. An anti-A,B antibody has also been identified, present only in group O individuals, which recognizes an epitope presumed to be common to the A and B antigens, which has yet to be identified.1 These ABO antibodies are “naturally” occurring, or “expected,” in contrast to antibodies to other blood group antigens, which are unexpected and usually stimulated by exposure through transfusion or pregnancy. They are stimulated in all immunocompetent individuals by environmental antigens, particularly bacteria. The normal intestinal flora carry polysaccharides similar to the A and B antigens, providing the stimulus for the formation of anti-A and anti-B.2 ABO antibodies are usually high titer and predominantly IgM with some IgG and IgA. They are capable of binding complement and causing intravascular hemolysis, thus starting off the dangerous cascade of an acute hemolytic transfusion reaction (HTR), which could lead to shock, renal failure, disseminated intravascular coagulation, and even death. IgM is not capable of crossing the placenta, but the smaller amounts of IgG and IgA that are present can, and are capable of causing hemolytic disease of the fetus and newborn (HDFN), which is usually mild. This is most common in group O mothers with non–group O infants. The anti-A, anti-B, and anti-A,B present in group O individuals can have significant amounts of IgG; however, the HDFN is still typically mild because the ABO antigens, although present, are not fully developed on the RBCs. Also, the ABO tissue antigens provide additional targets for absorbing these antibodies.

The ABO genes are inherited in a codominant manner, with one allele inherited from each parent and both being expressed. The resulting prevalence of ABO blood groups differs in various populations (Table 3.2). This becomes important in transfusion requirements and for procuring blood, as well as in solid organ transplant.

MNS

After the ABO blood groups were discovered by Landsteiner in 1900, experiments were performed to identify other blood groups (Reid, 2009). The MNS system was the second blood group identified. The MN and S antigens are glycophorans on the RBC surface. M and N are glyphophoran A, and S and s are glycophoran B. Antigens S and s differ by only one amino acid. During erythrocyte development, glycophoran A is detected shortly after the Kell antigen. The genes encoding the MNS antigens are located on chromosome 4 (4q28.2-q13.1). Rare MNS antigens have resulted from mutations in the glycophoran A and glycophorin B genes. Antibodies to the MNS antigens account for only 5% or less of cases of hemolytic disease of the fetus and newborn. Anti-M and anti-N are not considered to be a cause of transfusion reactions. Most neonates affected with anti-MNS hemolytic disease have hyperbilirubinemia that is manageable with phototherapy. Cases where exchange transfusions were used have been reported.